title: A novel role for adipose ephrin-B1 in inflammatory response.
abstract: OBJECTIVE
  Ephrin-B1 (EfnB1) was selected among genes of unknown function in adipocytes or adipose tissue and subjected to thorough analysis to understand its role in the development of obesity.
  
  
  RESULTS
  EfnB1 mRNA and protein levels were significantly decreased in adipose tissues of obese mice and such reduction was mainly observed in mature adipocytes. Exposure of 3T3-L1 adipocytes to tumor necrosis factor-α (TNF-α) and their culture with RAW264.7 cells reduced EFNB1 levels. Knockdown of adipose EFNB1 increased monocyte chemoattractant protein-1 (Mcp-1) mRNA level and augmented the TNF-α-mediated THP-1 monocyte adhesion to adipocytes. Adenovirus-mediated adipose EFNB1-overexpression significantly reduced the increase in Mcp-1 mRNA level induced by coculture of 3T3-L1 adipocytes with RAW264.7 cells. Monocyte adherent assay showed that adipose EfnB1-overexpression significantly decreased the increase of monocyte adhesion by coculture with RAW264.7 cells. TNF-α-induced activation of extracellular signal-regulated kinase 1/2 (ERK1/2) was reduced by EFNB1-overexpression.
  
  
  CONCLUSIONS
  EFNB1 contributes to the suppression of adipose inflammatory response. In obesity, reduction of adipose EFNB1 may accelerate the vicious cycle involved in adipose tissue inflammation.
authors.affiliation: Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
authors.forename: Takuya
authors.initials: T
authors.lastname: Mori
authors.forename: Norikazu
authors.initials: N
authors.lastname: Maeda
authors.forename: Kana
authors.initials: K
authors.lastname: Inoue
authors.forename: Ryohei
authors.initials: R
authors.lastname: Sekimoto
authors.forename: Yu
authors.initials: Y
authors.lastname: Tsushima
authors.forename: Keisuke
authors.initials: K
authors.lastname: Matsuda
authors.forename: Masaya
authors.initials: M
authors.lastname: Yamaoka
authors.forename: Takayoshi
authors.initials: T
authors.lastname: Suganami
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Nishizawa
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Ogawa
authors.forename: Tohru
authors.initials: T
authors.lastname: Funahashi
authors.forename: Iichiro
authors.initials: I
authors.lastname: Shimomura
mesh_terms: D017667:Adipocytes / Q000378:metabolism; D000273:Adipose Tissue / Q000378:metabolism* / Q000473:pathology; D000818:Animals; D002448:Cell Adhesion / Q000235:genetics; D002460:Cell Line; D004789:Enzyme Activation; D036387:Ephrin-B1 / Q000235:genetics / Q000378:metabolism*; D005786:Gene Expression Regulation; D055785:Gene Knockdown Techniques; D007249:Inflammation / Q000235:genetics / Q000378:metabolism*; D008297:Male; D051379:Mice; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism; D048052:Mitogen-Activated Protein Kinase 3 / Q000378:metabolism; D008954:Models, Biological; D009000:Monocytes / Q000378:metabolism; D009765:Obesity / Q000235:genetics / Q000378:metabolism; D015434:Panniculitis / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism
chemical_list: D036387:Ephrin-B1; D012333:RNA, Messenger; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3